Heritable Type B Aortic Dissection Is Associated With Retrograde Dissection Following Thoracic Endovascular Aortic Repair
Zhanjiang Cao, Wayne Zhang, Sherene Shalhub.
University of Washington, Seattle, WA, USA.
Background: We previously noted a higher than expected retrograde type A aortic dissection (RTAD) post thoracic endovascular aortic repair (TEVAR) in individuals with familial TBAD (FTBAD). We aimed to evaluate RTAD in the context of heritable thoracic aortic disease and other known anatomic risk factors.
Methods: Clinical and administrative records were reviewed for patients who underwent TEVAR for TBAD between 2003 and 2017. The clinical, hereditary, anatomic, and procedural characteristics were compared between patients with and without RTAD post RTAD.
Results: A total of 117 patients met the inclusion criteria (77.8% male) with a mean TBAD age of 58.6+12.1 years and a median follow up of 5.9 (IQR 2.2-9.4 years). TEVAR was performed in the acute phase in 40% of the cases. RTAD developed in 9 patients (7.7%, 78% male, median days to RTAD 21 days). Patients with RTAD were younger compared to patients without RTAD though not significant (Table 1). There were no differences in the degree of graft oversizing, arch type, timing of TEVAR, or the size of the ascending aorta at the time of TEVAR between the two groups. RTAD developed in 20% (N=6) of patients with heritable TBAD compared to 4% (N=3) of patients with sporadic TBAD (P=.009). RTAD extended to the ascending aorta in 6 cases with associated rupture (4 underwent surgical repair and 2 died prior to repair). In three cases, RTAD extended to the proximal arch, managed medically, and remained stable on follow up. Overall, RTAD was the cause of death of three cases (33.3% mortality).
Conclusions: In this study, there were no differences in the usual anatomic risk factors for TEVAR related RTAD but there were differences in the biologic basis of TBAD. While syndromic TBAD is a known risk factor, non-syndromic familial TBAD is also a risk factor for TEVAR related RTAD. Evaluation of family history as part of the workup for heritable etiology of TBAD is recommended and further evaluation to association of RTAD is warranted.
Table 1
| Retrograde Aortic Dissection (N=9) | No Retrograde Aortic Dissection (N=108) | P | |
| Age of TBAD | 53.8+8.2 | 59+12.4 | .226 |
| Male | 7 (77.8) | 84 (77.8) | 1 |
| Age at TEVAR | 54.8+8.1 | 61.2+12.2 | .128 |
| Duration to TEVAR (days) | 246.7+457.9 | 834.9+1695.3 | .364 |
| Ascending Aorta Diameter (mm) | 38.6+4.3 | 38.6+5 | .941 |
| Oversizing % | 6.7+5.3 | 9.7+3.8 | .099 |
| Diameter of proximal graft (mm) | 34.9+3.9 | 36.1+3.8 | .377 |
| Landing zone diameter (mm) | 32.7+4 | 33+4.1 | .842 |
| TBAD type (% of type) | .002 | ||
| Syndromic TBAD | 2 (50) | 2 (50) | |
| Familial TBAD | 3 (13.6) | 19 (86.4) | |
| Sporadic TBAD | 4 (4.4) | 87 (95.6) | |
| Arch type (% of type) | .988 | ||
| 1 | 2 (7.4) | 25 (92.6) | |
| 2 | 3 (8.3) | 33 (91.7) | |
| 3 | 4 (8.3) | 44 (91.7) |
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